Association of Cardiac CT‐Derived Epicardial Adipose Tissue With Atrial Fibrillation in Patients Without Left Atrial Fibrosis as Defined by Endocardial Voltage Mapping

医学 心房颤动 内科学 心脏病学 纤维化 导管消融 烧蚀 心外膜脂肪组织 脂肪组织
作者
Aqeel Umar,Jeffrey Hocking,Sophia Z. Massin,Adrian Suszko,Bernd J. Wintersperger,Vijay S. Chauhan
出处
期刊:Journal of Cardiovascular Electrophysiology [Wiley]
标识
DOI:10.1111/jce.16566
摘要

ABSTRACT Introduction Epicardial adipose tissue (EAT) is often associated with atrial fibrosis, and both can provide the substrate for atrial fibrillation (AF). However, most AF patients have no evidence of left atrial (LA) fibrosis based on bipolar voltage mapping. We determined whether EAT differs in AF patients without LA fibrosis compared to matched controls without AF. Methods Patients undergoing cardiac CT before first‐time AF catheter ablation were prospectively enrolled. LA bipolar voltage mapping was performed, and patients were divided into ‐LVZ (LA low voltage zones < 5% of LA surface area; no fibrosis) and +LVZ (LA low voltage zones ≥ 5%; fibrosis). A control group without AF was matched to −LVZ patients. EAT was quantified on CT using standard signal thresholding to quantify total and regional volumes. AF patients were followed for 1‐year postablation to assess atrial arrhythmia (AA) recurrence. Results −LVZ ( n = 50) had higher total EAT volumes than matched controls ( n = 48) (79 [58–109] vs. 51 [37–73] cm³, p < 0.001), higher LA EAT (9 [6.3–12] vs. 4.2 [2.9–5.8] cm³, p < 0.001), higher posterior LA EAT (9.7 [6.4–12] vs. 5.9 [2.8–7.2] cm³, p < 0.001) and higher right atrial EAT (7.3 [5.1–9.9] vs. 4.8 [3.2–6.5] cm³, p < 0.001). These differences remained even after correcting EAT for BMI and LA volumes. There were no significant differences in EAT volumes between −LVZ and +LVZ ( n = 25). There was no significant association between EAT and AF recurrence postablation. Conclusion EAT volume is greater in AF patients without evidence of LA fibrosis compared to matched controls without AF. These findings support an association of EAT with AF pathogenesis even in the absence of LA fibrosis.
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